Estimating Cardiovascular Risk in HIV-Infected Patients

From the initial reports of HIV infections in 1981, substantial progress in the prevention, detection and treatment have led to a marked reduction in mortality. Among them, the use of highly active antiretroviral therapy (HAART) with the combination of multiple antiretroviral drugs acting in different phases of the viral cycle resulted in impressive reductions in transmission and infectious complications. This increase in survival led to a large and growing population of persons living with HIV (PLWH) as a chronic condition in a setting where other non-infectious complications became more common.

Among those novel conditions affecting PLWH, cardiovascular complications became the leading cause of morbidity and mortality, at least in countries with adequate access to care and widespread use of HAART. The increase in cardiovascular risk in PLWH is multifactorial. First, studies suggest that PLWH are more likely to be diabetics and smokers. Second, those individuals are more likely to have higher triglycerides and lower HDL-C, though LDL-C and total cholesterol were also reduced. It also seems possible that HIV infection is responsible for increases in blood pressure and glucose levels by different mechanisms. However, considerable evidence supports the concept that traditional risk factors do not fully account for the higher cardiovascular risk in those individuals, as the changes in the cardiovascular system in PWLH is multifactorial and at least partially mediated by inflammation and immune activation, leading to endothelial dysfunction, changes in vascular elasticity, coagulation.

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